Frostbite, or freezing cold injury, remains a significant but often underappreciated form of environmental trauma. It occurs when cutaneous and subcutaneous tissues are exposed to temperatures below 0°C, leading to ice crystal formation, microvascular thrombosis, and progressive ischemia. While historically associated with military operations, frostbite now most commonly affects homeless individuals, winter sports enthusiasts, and those with behavioral or medical risk factors such as alcohol use, malnutrition, diabetes, or peripheral vascular disease. The pathophysiology follows a predictable pattern: initial vasoconstriction, endothelial damage, hyperviscosity, and ultimately tissue necrosis unless timely rewarming is achieved. Clinically, frostbite is staged from first-degree (numbness and erythema) to fourth-degree (deep tissue loss and autoamputation). Management has evolved significantly. In the field, the priority is to protect from further injury, avoid refreezing, and initiate gentle rewarming only when refreezing is not a risk. In-hospital care includes controlled warm-water immersion at 40–42°C, aggressive pain control with NSAIDs and narcotics, careful blister management, delayed debridement, and, in select severe cases, thrombolytic therapy with tPA or iloprost. The single most important prognostic principle is patience: amputation should be delayed for weeks to allow spontaneous demarcation of viable tissue. Long-term sequelae include cold intolerance, chronic pain, complex regional pain syndrome, and functional deficits. Prevention through education—proper clothing, hydration, avoidance of alcohol and tobacco—remains the most effective intervention. An interprofessional team approach, involving emergency medicine, surgery, wound care, and rehabilitation, optimizes outcomes.